Exposure to Air Pollution May Raise Hypertension Risk

Both acute and chronic exposure linked to higher BP risk

Action Points

Both short-term exposure (to sulfur dioxide), and long-term exposure (to nitrogen oxide) were linked to an increased risk for high blood pressure in a meta-analysis.

Note that exosure to other ambient air pollutants (short-term exposure to NO2, O3, and CO and long-term exposure to NOx, PM2.5, and SO2) also had positive relationships with hypertension, but lacked statistical significance, possibly due to the small number of studies.

Both short- and long-term exposure to some air pollutants, but not others, was linked to an increased risk for high blood pressure in a meta-analysis of 17 previously published studies totalling more than 300,000 participants.

Short-term exposure to sulfur dioxide and particulate matter and long-term exposure to nitrogen oxide and particulate matter were all significantly associated with elevated high blood pressure risk in the analysis, while significant associations were not seen for ozone and carbon monoxide exposure.

The study is among the first meta-analyses to simultaneously estimate the effects of short- and long-term exposure to air pollutants on hypertension, researcher Tao Liu, PhD, of the Guandong Provincial Institute of Public Health, Guandong, China, and colleagues wrote in the journal Hypertension, published online May 31.

And the pooled study findings are in agreement with many published studies suggesting a link between exposure to air pollution and cardiovascular disease, said American Heart Association spokesperson Martha Daviglus, MD, PhD, of the University of Illinois College of Medicine in Chicago, who was not involved with the research.

"The findings are not a surprise, but the fact that the study is a meta-analysis, with greater statistical power, adds to the strength of this association," she told MedPage Today.

Most individual studies evaluating the impact of air pollution exposure on blood pressure have examined either the acute or chronic effects of exposure, but not both.

"The short-term and long-term effects of air pollution may have non-mutually exclusive biological mechanisms, that is, direct and indirect effects on the sympathetic nervous system, oxidative stress, endothelial and other hemodynamic function, and vascular tone," the researchers wrote.

Their systemic review included all studies published before September of 2015 examining the association between ozone (O3); carbon monoxide (CO), nitrogen oxide (NO2 and NOx), sulfur dioxide (SO2), and particulate matter (PM10 and PM2.5) with hypertension. The analysis included data on more than 108,000 patients with hypertension and 220,000 nonhypertensive controls.

Pooled odds ratio for hypertension in association with each 10 µg/m3 increase in air pollution was calculated using a random-effects model for studies with significant heterogeneity, or a fixed-effect model for studies without significant heterogeneity.

A total of 17 studies were included in the analysis, examining the effects of short-term (n=6) and long-term exposure (n=11) to air pollutants.

Exposure to other ambient air pollutants (short-term exposure to NO2, O3, and CO and long-term exposure to NOx, PM2.5, and SO2) also had positive relationships with hypertension, but lacked statistical significance, possibly due to the small number of studies examining these pollutants resulting in low statistical power.

Possible mechanisms by which air pollution contributes to hypertension risk include the promotion of inflammation and oxidative stress, the researchers noted.

"Our results provide strong evidence that both short-term and long-term exposure to the main air pollutants increases the risk of hypertension," they wrote. "Our findings are of public health importance because both air pollution and hypertension are important worldwide public health problems."

Liu and colleagues cited several study limitations, including the paucity of studies examining the impact of CO and O3 exposure, which prevented them from conducting a meta-analysis, as well as limited data on other pollutants.

"We cannot rule out the possibility that our current results are chance findings and that the absence of publication bias is because of the relatively small number of included primary studies," they wrote.

Daviglus said more research is needed to better understand the role of individual pollutants on hypertension risk, but she added that there is little doubt that exposure to air pollution, in general, raises cardiovascular disease risk.

She said while the public health concern is clear, the message to individual patients is more complicated.

"We can't really tell patients, 'Move to a cleaner city' or 'Don't leave your house.' That just isn't practical," she said. "The best advice we can give is to tell them to do the things that we know lower cardiovascular risk. Don't smoke, eat a healthy diet, exercise and keep your weight down."

Funding for this research was provided by the National Natural Science Foundation of China, the Natural Science Foundation of Guangdong Province and the Postdoctoral Science Foundation of China.

The researchers declared no relevant relationships with industry related to this research.

Reviewed by Robert Jasmer, MD Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner

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